ArticleLeukemia2022
MiRNA-363-3p/DUSP10/JNK axis mediates chemoresistance by enhancing DNA damage repair in diffuse large B-cell lymphoma.
Article in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- PRMT7-mediated arginine methylation of FOXK activates Wnt/β-catenin signalling to drive doxorubicin resistance in diffuse large B-cell lymphoma.Clinical and translational medicine · 2026Article
- Exosomal miRNA as a biomarker for diagnosis and prognosis, and a new target for regulating treatment resistance in DLBCL: a research progress narrative review.Translational cancer research · 2026Review
- ATF3 Modulates the Endoplasmic Reticulum Stress-Induced Impairment of Milk Synthesis in Bovine Mammary Epithelial Cells.International journal of molecular sciences · 2026Article
- Extracellular vesicles as regulators of chemotherapy resistance in oral squamous cell carcinoma.Discover oncology · 2026Review
- Dual Metabolic Inhibition by Berberine and Glutor Triggers AMPK/JNK-Dependent DNA Damage in Cancer Cells.International journal of medical sciences · 2026Article
- Mechanisms of first-line treatment resistance in diffuse large B-cell lymphoma.Frontiers in immunology · 2026Review
- Advances in epigenetic therapies for B-cell non-hodgkin lymphoma.Annals of hematology · 2024Review
- ARMC10 regulates mitochondrial dynamics and affects mitochondrial function via the Wnt/β-catenin signalling pathway involved in ischaemic stroke.Journal of cellular and molecular medicine · 2024Article
- Epigenetic alterations and advancement of lymphoma treatment.Annals of hematology · 2024Review
- Molecular panorama of therapy resistance in prostate cancer: a pre-clinical and bioinformatics analysis for clinical translation.Cancer metastasis reviews · 2024Review
- PRPF19 functions in DNA damage repair and gemcitabine sensitivity via regulating DDB1 in bladder cancer cells.Cytotechnology · 2024Article
- Hypoxia-regulated secretion of IL-12 enhances antitumor activity and safety of CD19 CAR-T cells in the treatment of DLBCL.Molecular therapy oncolytics · 2023Article
- Mesenchymal stem cells, as glioma exosomal immunosuppressive signal multipliers, enhance MDSCs immunosuppressive activity through the miR-21/SP1/DNMT1 positive feedback loop.Journal of nanobiotechnology · 2023Article
- A Brief Review on Chemoresistance; Targeting Cancer Stem Cells as an Alternative Approach.International journal of molecular sciences · 2023Review
- TRAF4-mediated ubiquitination-dependent activation of JNK/Bcl-xL drives radioresistance.Cell death & disease · 2023Article
- Role of microRNA alternation in the pathogenesis of gouty arthritis.Frontiers in endocrinology · 2022Review
- microRNAs associated with the pathogenesis and their role in regulating various signaling pathways duringFrontiers in cellular and infection microbiology · 2022Review
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anthracycline-based chemotherapy resistance represents a major challenge in diffuse large B-cell lymphoma (DLBCL). MiRNA and gene expression profiles (n = 47) were determined to uncover potential chemoresistance mechanisms and therapeutic approaches. An independent correlation between high expression of miRNA-363-3p and chemoresistance was observed and validated in a larger cohort (n = 106). MiRNA-363-3p was shown to reduce doxorubicin-induced apoptosis and tumor shrinkage in in vitro and in vivo experiments by ectopic expression and CRISPR/Cas9-mediated knockout in DLBCL cell lines. DNA methylation was found to participate in transcriptional regulation of miRNA-363-3p. Further investigation revealed that dual specificity phosphatase 10 (DUSP10) is a target of miRNA-363-3p and its suppression promotes the phosphorylation of c-Jun N-terminal kinase (JNK). The miRNA-363-3p/DUSP10/JNK axis was predominantly associated with negative regulation of homologous recombination (HR) and DNA repair pathways. Ectopic expression of miRNA-363-3p more effectively repaired doxorubicin-induced double-strand break (DSB) while enhancing non-homologous end joining repair and reducing HR repair. Targeting JNK and poly (ADP-ribose) polymerase 1 significantly inhibited doxorubicin-induced DSB repair, increased doxorubicin-induced cell apoptosis and tumor shrinkage, and improved the survival of tumor-bearing mice. In conclusion, the miRNA-363-3p/DUSP10/JNK axis is a novel chemoresistance mechanism in DLBCL that may be reversed by targeted therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.